Although cardiovascular structure and systolic and diastolic cardiac properties are altered in advanced age, the most striking and consistent observation is that these alterations are neither uniform nor inexorable. Thus, while the average heart undergoes mild hypertrophy, and evidences slowed and delayed relaxation at rest, and diminished performance during exercise stress, some do not. Although left ventricular mass, early diastolic filling, and exercise contractile performance changes are age-related, the relationship may not be due to aging alone but, in addition, to other factors which co-vary with age. If this is true, modification of these other factors may retard, inhibit, or even reverse previously described "age-associated" changes. Excluding hypertension and ischemic heart disease, the most important of these are lifestyle factors, particularly physical activity status. The hypothesis of this proposal is that physical activity status has a significant modifying influence on previously described "age-associated" cardiovascular alterations. The objective is to determine the extent to which altering physical activity status in lean elderly, disease-free individuals will alter their cardiac structure and function. The specific aims of the proposal are to assess in elderly individuals without evidence of overt or latent cardiovascular disease the influence on cardiac structure and function of physical activity status, as indexed by maximal aerobic capacity, and changes in that status. Cardiac structure will be determined by magnetic resonance imaging and indexed by left ventricular mass, and regional left ventricular wall thickness and area. Cardiac function will be determined by using resting 2-D Echo and Doppler and resting and exercise gated blood pool scans and indexed by ejection fraction, cardiac output, left ventricular volumes, oxygen consumption, diastolic filling rates, and left ventricular systolic wall thickening. This proposal will therefore assess the impact of physical activity status on previously described "age-associated" changes in cardiovascular structure and function in elderly, disease-free subjects.